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Aging and disease    2019, Vol. 10 Issue (5) : 1075-1093     DOI: 10.14336/AD.2018.0815-1
Review Article |
Preclinical Evidence and Possible Mechanisms of Extracts or Compounds from Cistanches for Alzheimer’s Disease
Xiao-Li Zhou, Meng-Bei Xu, Ting-Yu Jin, Pei-Qing Rong, Guo-Qing Zheng*, Yan Lin*
Department of Neurology, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China
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Abstract  

Currently, disease-modified strategies to prevent, halt or reverse the progress of Alzheimer’s disease (AD) are still lacking. Previous studies indicated extracts or compounds from Cistanches (ECC) exert a potential neuroprotective effect against AD. Thus, we conducted a preclinical systematic review to assess preclinical evidence and possible mechanisms of ECC in experimental AD. A systematical searching strategy was carried out across seven databases from their inceptions to July 2018. Twenty studies with 1696 rats or mice were involved. Neurobehavioral function indices as primary outcome measures were established by the Morris water maze test (n = 11), step-down test (n = 10), electrical Y-maze test (n = 4), step-through test (n = 3), open field test (n = 2) and passage water maze test (n = 1). Compared with controls, the results of the meta-analysis showed ECC exerted a significant effect in decreasing the escape latency, error times and wrong reaction latency in both the training test and the retention test, and in increasing the exact time and the percentage of time in the platform-quadrant and the number of platform crossings (all P<0.01). In conclusion, ECC exert potential neuroprotective effects in experimental AD, mainly through mechanisms involving antioxidant stress and antiapoptosic effects, inhibiting Aβ deposition and tau protein hyperphosphorylation and promoting synapse protection. Thus, ECC could be a candidate for AD treatment and further clinical trials.

Keywords Cistanches      Alzheimer’s disease      dementia     
Corresponding Authors: Zheng Guo-Qing,Lin Yan   
About author:

Present address: Department of Neurology, National Neuroscience Institute, Tan Tock Seng Hospital, Singapore.

Issue Date: 27 September 2019
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Zhou Xiao-Li
Xu Meng-Bei
Jin Ting-Yu
Rong Pei-Qing
Zheng Guo-Qing
Lin Yan
Cite this article:   
Zhou Xiao-Li,Xu Meng-Bei,Jin Ting-Yu, et al. Preclinical Evidence and Possible Mechanisms of Extracts or Compounds from Cistanches for Alzheimer’s Disease[J]. Aging and disease, 2019, 10(5): 1075-1093.
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http://www.aginganddisease.org/EN/10.14336/AD.2018.0815-1     OR     http://www.aginganddisease.org/EN/Y2019/V10/I5/1075
Figure 1.  Summary of the process for identifying candidate studies.
Figure 2.  The forest plot in Morris water maze test. Effects of ECC for (A) decreasing the escape latency in spatial performance, increasing (B) exact time/(C) percentage of time and (D) increasing crossing numbers in platform-quadrant in probe test compared with control group.
Study (years)Type of herbal or bioactive compoundSpecies
Sex Weight N
AnestheticModel
(method)
Experimental groupControl groupOutcome measureIntergroup differences*
Kuang, 2009GCsKM mice
M 18-22g 75
-D-gal and sodium nitriteGCs (60, 120 mg/kg)
ig, 40~50d
NS for same volume1. Step-down test
1.1.1 error number (T) 1.1.2 wrong react latency (T) 1.2.1 error number (RT) 1.2.2 wrong react latency (RT) 2. Step-through test 2.1.1 error number (T) 2.1.2 latency (T) 2.2.1 error number (RT) 2.2.2 latency (RT) 3. Morris water maze test escape latency

1.1.1 P<0.05 1.1.2 P>0.05 1.2.1 P<0.05 1.2.2 P>0.05 2.1.1 P<0.05 2.1.2 P>0.05 2.2.1 P<0.05 2.2.2 P<0.05 3. P<0.01
KM mice
M 18-22g 50
-D-gal and sodium nitriteGCs (60, 120 mg/kg)
ig, 40~50d
NS for same volume4. Na+-K+ ATPase
5. GSH-PX
4. P<0.05
5. P<0.001
SD rat
M 180-200g 40
-D-gal and sodium nitriteGCs (60, 120 mg/kg)
ig, 40~50d
NS for same volume6. SOD
7. NO
6. P<0.001
7. P<0.01
Wu, 2014GCsSD rats
M 300-350g 100
phenobarbitalAβ (1-42)GCs (100, 200 mg/kg)
ig, 7-14d
a. sterile distilled water for same volume
b. donepezil (0.75 mg/kg)
1.Open field test
1.1 time spend in the hole 1.2 number of entries 1.3 movement activity 2.Step-through test latency (T) 3. Morris water maze test 3.1 escape time 3.2 exact time in platform-quadrant 3.3 swimming velocity 4. Aβ (1-42) deposition 5. Neurotransmitters and metabolites (ACh, NE, DA) 6. Activity of AChE, MAO-A and MAO-B
1.1 P>0.05
1.2 P>0.05 1.3 P>0.05 2. P<0.001 3.1 P<0.05 3.2 P<0.001 3.3 P>0.05 4. P<0.01 5. P<0.05 6. P<0.05
Liu, 2005GCsKM mice
M 20-24g 60
chloral hydrateQuinolinic acidGCs (62.5, 125, 250 mg/kg)
ig, 15d
sterile distilled water for same volume1.Step-down test
1.1 error number (T) 1.2 error number (RT) 2. Electrical Y- maze test right react times 3. Activity of SOD, MDA and GSH-PX. 4. Neuron apoptosis 5. Calcium content
P<0.05
P<0.05 2. P<0.05 3. P P<0.05 or P<0.01 4. P<0.01 5. NG
Liu, 2006GCsNIH mice
M 20-24g 60
chloral hydrateAβ (25-35)GCs (62.5, 125, 250 mg/kg)
ig, 17d
sterile distilled water for same volume1. Step-down test
1.1 error number (T) 1.2 error number (RT) 2. Activity of SOD, MDA and GSH-PX 3. Neuron apoptosis 4. Bax / Bcl-2

P<0.01 P<0.01 2. P<0.05 or P<0.01 3. P<0.01 4. NG
Luo, 2007GCsKM mice
M 20-24g 60
chloral hydrateAlCl3GCs (62.5, 125, 250 mg/kg)
ig, 20d
NS for same volume1. Step-down test
1.1 error number (T) 1.2 wrong react latency (T) 2. Electrical Y-maze test error react times 3. Activity of SOD and MDA 4. Brain weight coefficient

1.1 P<0.05 1.2 P<0.05 2. P<0.01 3. P<0.05 or P<0.01 4. P<0.01
Luo, 2013GCsSD rats
M 220-270g 60
chloral hydrateAβ (25-35)GCs (40, 80, 120 mg/kg)
ig, 14d
NS for same volume1. Step-down test
1.1 error number (T) 1.2 reaction time (T) 2. Electrical Y-maze test error react times 3. Activity of AchE 4. Calcium content

1.1 P<0.01 1.2 P<0.01 2. P<0.01 3. P<0.01 4. NG
Yin, 2013(A)CDPSSD rats
M/F 200-250g 60
chloral hydrateAβ (25-35)CDPS (20, 40, 80 mg/kg)
ig, 28d
NS for same volume1. Morris water maze test
escape latency 2. Neuron apoptosis 3. Expression of Bcl-2 and caspase-3
1. P<0.01
2. P<0.01 3. P<0.01
Yin, 2013(B)CDPSWistar rats
NG 180-220g 60
chloral hydrateAβ (1-40)CDPS (L, M, H)
ig, 28d
corn oil for same volume1. Morris water maze test
escape latency 2. Activity of SOD and MDA 3. Activity of NO, ONOO- and ROS
1. P<0.01
2. P P<0.05 or P<0.01 3. P<0.05 or P<0.01
Li, 2011CDPSKM mice
M/F 18-22g 75
-ScopolamineCDPS (10, 20, 60 mg/kg)
NG
NS for same volume1. Passage water maze test
1.1 error number (T) 1.2 latency (T) 2. Morris water maze test escape latency 3. Activity of SOD, MDA and AChE
P<0.01
P<0.01 2. P<0.05 3. P<0.05 or P<0.01
Ding, 2014ECHSD rats
M 290-320g 60
chloral hydrateD-gal and Aβ (25-35)ECH (10, 20, 40 mg/kg)
ig, 28d
a. NS for same volume
b. huperzine-A (0.02 mg/kg)
1. Morris water maze test
1.1 escape latency 1.2 number of platform crossing 1.3 exact time in platform-quadrant 2. Activity of NE, DA and 5-TH

1.1 P<0.01 1.2 P<0.01 1.3 NG 2. P<0.05
Peng, 2014ASKM mice
F 16-20g 120
-D-gal and AlCl3AS (30, 60, 120 mg/kg)
ig, 30d
NS (10 ml/kg)1. Step-down test
1.1.1 error number (T) 1.1.2 wrong react latency (T) 1.2.1 error number (RT) 1.2.2 wrong react latency (RT) 2. Level of NO 3.Pathomorphological changes in the hippocampus 4. Expression of Caspase-3

1.1.1 P<0.01 1.1.2 P>0.05 1.2.1 P<0.01 1.2.2 P>0.01 2. P<0.01 3. NG 4. P<0.05
Hu, 2016ASAPP/PSI mice
NG 25-35g 40
--AS (30, 60, 120 mg/kg)
ig, 60d
sterile distilled water for same volume1.Morris water maze test
1.1 escape latency 1.2 number of platform crossing 1.3 percentage of time in platform-quadrant 2. Neuron apoptosis 3. Survival neuron number 4. Aβ (1-42) deposition

1. 1 P<0.01 1.2 P<0.05 1.3 P<0.01 2. P<0.05 3. P<0.05 4. P<0.05
Jia, 2014GCs10-month-old SAMP8 mice
M 25-35g 40
--GCs (100 mg)
ig, 30d
NS for same volume1. Morris water maze test
1.1 escape latency 1.2 number of platform crossing 1.3 time in the target quadrant 1.4 swimming speed 2. Survival neuron number 3. Activity of MDA, SOD and GSH-PX
1. 1 P<0.01
1.2 P<0.01 1.3 P<0.01 1.4 P>0.05 2. P<0.01 3. P<0.05 or P<0.01
Jia, 2017PhG10-month-old SAMP8 mice
M 30g 40
--PhG (25, 50, 100 mg/kg)
ig, 30d
NS for same volume1. Morris water maze test
1.1 escape latency 1.2 number of platform crossing 1.3 percentage of time in platform-quadrant 1.4 path length 2. Activity of MDA, SOD and GSH-PX 3.Density of dendritic spines 4.Expression of SYN and PSD-95

P<0.05 P<0.05 P<0.05 P<0.05 2. P<0.05 or P<0.01 3. P<0.05 4. P<0.05
Gao, 2005GCsKM mice
M/F 18-22g 180
-ScopolamineGCs (L, M, H)
ig, 30d
sterile distilled water for same volume1. Step-down test
1.1 error number (T) 1.2 wrong react latency (T)
P<0.01
1.2 P<0.01
Wu, 2017CDPSKM mice
M/F 18-22g 192
-D-galCDPS (25, 50, 100 mg/kg)
ig, 42d
NS for same volume1. Morris water maze test
1.1 escape latency 1.2 number of platform crossing
P<0.05
P<0.05
Yin, 2014CDPSKM mice
M/F 23-27g 72
-ScopolamineCDPS (25, 50, 100 mg/kg)
ig, 42d
a. sterile distilled water for same volume
b. donepezil (0.8 mg/kg)
Morris water maze test
1.1 escape latency 1.2 exact time in platform-quadrant 1.3 path length 2. Step-down test 2.1.1 error number (T) 2.1.2 right latency (T) 2.2.1 error number (RT) 2.2.2 right latency (RT) 3. Expression of GAP-43 and SYP 4. Number and morphology of synapses

1.1 NG 1.2 P<0.05 1.3 NG 2.1.1 P<0.05 2.1.2 P>0.05 2.2.1 P<0.05 2.2.2 P<0.05 3. P<0.05 4. P<0.05
Shiao, 2017ECHSD rat
M 300-350 120
phenobarbitalAβ (1-42)/ ScopolamineECH (2.5, 5.0 mg/kg)
ig, 15d
a. sterile distilled water for same volume
b. donepezil (0.75 mg/kg)
1. Open-field task
1.1 time spend in the hole 1.2 number of entries into the hole 1.3 movement activity 2. Step-through test 2.1 latency (T) 2.2 latency (RT) 3. Morris water maze test 3.1 escape latency 3.2 exact time in platform-quadrant 3.3 swimming velocity 4. Aβ (1-42) deposition 5. Levels of Ach, NE and DA 6. Activity of AChE, MAO-A and MAO -B

1.1 P<0.05 1.2 P<0.05 1.3 P>0.05 2.1 P<0.05 2.2 P>0.05 3.1 P<0.05 3.2 P<0.05 3.3 P>0.05 4. P<0.05 5. P<0.05 or P<0.01 6. P<0.05 or P<0.01
Piao, 2001ASKM mice
M 18-22 60
-ScopolamineAS (5, 10 mg/kg)
ig, 10d
a. NS for same volume
b. huperzine-A (0.07 mg/kg)
1. Step-down test
1.1.1 wrong react latency (T) 1.1.2 error time (T) 1.2.1 wrong react latency (RT) 1.2.2 error time (RT) 2. Electrical Y-maze test right react times 3. Activity of AChE

1.1.1 NG 1.1.2 P>0.05 1.2.1 P<0.05 1.2.2 P<0.05 2. P<0.05 3. P<0.05
Lin, 2012ASKM mice
M 18-22g 72
-ScopolamineAS (30, 60, 120mg/kg)
ig, 10d
a. NS for same volume
b. huperzine-A (0.07 mg/kg)
1. Step-down test
1.1.1 error number (T) 1.1.2 wrong react latency (T) 1.2.1 error number (RT) 1.2.2 wrong react latency (RT) 2. Activity of MDA, SOD and GSH-PX 3. Protein content in brain tissue

1.1.1 NG 1.1.2 NG 1.2.1 P<0.01 1.2.2 P<0.01 2. P<0.05 or P<0.01 3. P>0.05
Table 1  Characteristics of the included studies.
Figure 3.  The forest plot in Step-down test. Effects of ECC for decreasing (A) error times and (B) wrong react latency in training test and decreasing (C) error times and (D) wrong react latency in retention test compared with control group.
Figure 4.  The forest plot in Electrical Y-maze test and Step-through test. Effects of ECC for (A) decreasing error react times, (B) increasing right react times in Electrical Y-maze test, and decreasing latency in training test (C) / retention test (D) in Step-through test compared with control group.
Figure 5.  The forest plot of oxidative stress. Effects of ECC for increasing the activity of (A) SOD and (C) GSH-Px, decreasing (B) MDA and (D) NO compared with control group.
Figure 6.  The forest plot of AChE and neurotransmitters. Effects of ECC for (A) decreasing the activity of AChE, increasing the level of Ach in hippocampus (B)/in cortex (C), increasing the level of DA in hippocampus (D)/in cortex (E), increasing the level of NE in hippocampus (F)/in cortex (G), and decreasing the activity of MAO-A in hippocampus (I)/in cortex (H) compared with control group.
StudyABCDEFGHITotal
Kuang, 2009-++-+--++5
Wu, 2014+++----++5
Liu, 2005+-+-+---+4
Liu, 2006+-+-+---+4
Luo, 2007+-+-+---+4
Luo, 2013+---+---+3
Yin, 2013 (A)+-+-++--+5
Yin, 2013 (B)+-+-+?--+3
Li, 2011+-+-++-++6
Ding, 2014+++-+--++6
Peng, 2015+++-++-++7
Hu, 2016+++-+?-++6
Jia, 2014+++-++-++7
Jia, 2017+++-++-++7
Gao, 2005+-+-++--+5
Wu, 2017+-+-++-++6
Yin, 2014+-+-++--+5
Shiao, 2017+++----++5
Piao, 2001+-+-+---+4
Lin, 2012+-+-+---+4
Table 2  Risk of bias of the included studies.
Figure 7.  The forest plot of neuropathologic changes and Caspase-3. Effects of ECC for (A) decreasing Aβ deposition, (B) decreasing apoptosis and (C) decreasing Caspase-3compared with control group.
Figure 8.  Summary of the possible neuroprotective mechanism of ECC for AD. ECC reduced the excessive ROS in mitochondrion, increased the activity of GSH-PX, SOD, and decreased the level NO and MDA. ECC decreased the level NO, down-regulated the over activation of microglia, exerting potential inhibitory effects on microglia-involved neuro-inflammation. ECC decreased Aβ deposition and tau protein hyper-phosphorylation. ECC decreased the activity of AchE and maintained the normal level of Ach and NE in Cholinergic neuron and increased the level of DA in hippocampus. ECC activated the NMDA -receptor and ameliorated the loss of synapses. The evidence of ECC in increasing the level of 5-HT is inadequate currently. ECC regulate the calcium deposition and maintain neuronal calcium homeostasis. ECC up-regulate the expressions of Bcl-2, decrease the ratio of Bax / Bcl2, down-regulate the expressions of Caspase-3 and reduce neurocyte apoptosis.
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